Cardiovascular toxicities associated with immune checkpoint inhibitors

Cardiovasc Res. 2019 Apr 15;115(5):854-868. doi: 10.1093/cvr/cvz026.


Cardiovascular toxicities associated with immune checkpoint inhibitors (ICIs) have been reported in case series but have been underappreciated due to their recent emergence, difficulties in diagnosis and non-specific clinical manifestations. ICIs are antibodies that block negative regulators of the T cell immune response, including cytotoxic T lymphocyte-associated protein-4 (CTLA-4), programmed cell death protein-1 (PD-1), and PD-1 ligand (PD-L1). While ICIs have introduced a significant mortality benefit in several cancer types, the augmented immune response has led to a range of immune-related toxicities, including cardiovascular toxicity. ICI-associated myocarditis often presents with arrhythmias, may co-exist with myositis and myasthenia gravis, can be severe, and portends a poor prognosis. In addition, pericardial disease, vasculitis, including temporal arteritis, and non-inflammatory heart failure, have been recently described as immune-related toxicities from ICI. This narrative review describes the epidemiology, diagnosis, pathophysiology, and treatment of cardiovascular toxicities of ICI therapy, highlighting recent developments in the field in the past year.

Keywords: Cardio-oncology; Cardiovascular toxicity; Immune checkpoint inhibitors; Myocarditis; Pericarditis; Vasculitis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents, Immunological / adverse effects*
  • Cardiotoxicity
  • Cardiovascular Diseases / chemically induced*
  • Cardiovascular Diseases / diagnosis
  • Cardiovascular Diseases / physiopathology
  • Cardiovascular Diseases / therapy
  • Humans
  • Myocarditis / chemically induced
  • Neoplasms / drug therapy*
  • Neoplasms / immunology
  • Neoplasms / pathology
  • Pericarditis / chemically induced
  • Prognosis
  • Risk Assessment
  • Risk Factors
  • Vasculitis / chemically induced


  • Antineoplastic Agents, Immunological